Force Transmission by Minimal Focal Adhesion Complexes Induces Synthetic Cell Deformation

TL;DR

Researchers created a synthetic system to study how cells transmit forces through focal adhesion proteins, showing that minimal components can deform cell-like structures.

Contribution

A minimal synthetic system reconstituting focal adhesion complexes in GUVs to study force transmission and mechanosensing.

Findings

Defined protein-membrane interactions can nucleate actin networks and anchor them to membranes.

Actomyosin contraction leads to structural alignment and deformation of GUVs.

The system remains stable under load, demonstrating force transmission and mechanosensing capabilities.

Abstract

Cells sense and respond to mechanical cues through focal
adhesions–dynamic,
multiprotein assemblies linking the actin cytoskeleton to the extracellular
matrix. These complexes are essential to processes from cell migration
to tissue morphogenesis, yet the minimal physical requirements for
their force-transmitting and mechanosensing functions remain unclear.
Here, we reconstitute minimal focal adhesion-like complexes in giant
unilamellar vesicles (GUVs) using kindlin-2, talin-1, FAK, paxillin,
zyxin, and VASP anchored to membranes containing PIP2 and
integrin β1 tails. These assemblies nucleate and anchor actin
filaments into networks spanning the vesicle surface. Upon addition
of nonmuscle myosin IIa, actomyosin contraction thickens filament
bundles, aligns the complexes, and deforms the GUVs, while the assemblies
remain stably membrane-bound. Our findings show that actin recruitment,
force transmission, and structural stability under load can emerge
from defined protein-membrane interactions alone. This minimal, three-dimensional
platform offers a controllable synthetic biology system for probing
mechanosensing and engineering force-responsive biomimetic systems.

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